Book 2 Listening (1108796), страница 21
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In April three teams of researchers identified specific mutations that increasethe chance of autism; all three observed that the risk of such mutations in a child rose withhis father's age at conception. But Dr Stefansson and his team are the first to measure theimpact of older fathers so precisely.74Modern genomics made their task easier. After sequencing the genomes of each of thepeople involved, tallying the new mutations in the children was simply a matter of comparingthe sequences of the parents with those of their offspring. Though both mother and fathercontribute to a child's DNA, their contributions come in large, identifiable blocks. If a mutationis seen, its parentage is thus obvious.There is, of course, the question of how much this matters, for most mutations have littleeffect - and a rare few, the stuff of evolution, are actually beneficial.
According to AlexeyKondrashov of the University of Michigan, an expert on the matter who wrote an article inNature to accompany Dr Stefansson's study, about 10% of mutations are damaging. Thismeans that for the average baby, six of Dr Stefansson's 63 mutations are probably up to nogood.In Iceland, the average age of fathers at conception has risen from 28 in 1980 to 33 in2011. Over the same period Dr Stefansson estimates that the number of new mutations inIceland's newborns jumped by more than 17%.Whether that has implications for the country's overall health remains to be seen.
In thegrand scheme of things, the negative effect of extra mutations is likely to be countervailed bythe positive effects of modern life: better nutrition, hygiene and sanitation, as well as bettermedical care. But Dr Stefansson's results do give pause for thought. Some women - thoseundergoing cancer-related hysterectomy, for example - have eggs frozen before theiroperations.
In the fullness of time, perhaps men will think likewise and have some of thesperm of their carefree, mutation-free youths frozen in case they fancy a little procreation intheir old age. (From The Economist, August 25, 2012)75Unit 14. AgingScript 42. Stress and ageing.A question of attitudeThe link between chronic stress and a marker of old age is being disentangledTelomers are to chromosomes what plastic caps are to shoelaces- they stop themfraying at the ends. Unlike shoelaces, though, chromosomes replicate themselves from timeto time as the cells they are in divide. This shortens the telomere and, after 50-to-70 suchdivisions (a number known as the Hayflick limit, after its discoverer), a chromosome can growno shorter and the cell it is in can divide no more.That provides a backstop against cancer.
The rapidly dividing cells in a tumour soon hitthe Hayflick limit and the process is brought to a screeching halt. Which is a good thing. Thebad thing is that reaching the limit is one of the markers of old age. You do not want it tohappen too quickly, particularly in tissues that have to do a lot of dividing in order to workproperly, such as those in the immune system.It has been known for some time that chronic stress (caring for a child with a protractedillness, for example) causes premature shortening of the telomeres. What has not been clearis whether this is a one-way trip, with each stressful period turning the telomeric ratchetirreversibly.
This week, though, at a meeting of the American Association for CancerResearch in Orlando, Florida, a group of researchers led by Edward Nelson of the Universityof California, Irvine, showed that it isn't. Their research suggests that stress management notonly stops telomeres from shortening, it actually promotes their repair.Dr Nelson drew this welcome conclusion from a previous study that measured theimpact of telephone counselling on women who had been treated for cervical cancer. Thestudy found that such counseling worked, both mentally and physically.
Women who hadbeen counselled reported that the quality of their lives had improved, compared with those ofa control group who had not been counselled. They also showed improvements in thestrength of their immune systems.Given those benefits, Dr Nelson wondered if he could find others, and he re-examinedthe participants' samples to look at the lengths of the telomeres in their white blood cells (redcells have no nuclei, and therefore no chromosomes).
What he found surprised him. Not onlydid counseling stop telomere shrinkage, it actually promoted telomere growth. Those womenfor whom counselling had worked (ie, those who reported a decrease in emotional stress)had longer telomeres at the end than they did at the beginning. Their Hayflick countdownswere being reset.A single such result must, of course, be treated with caution. But another study reportedat the meeting, by Elizabeth Blackburn of the University of California, San Francisco (whoshared the Nobel prize for the discovery of the enzyme that repairs telomeres), gave somesupport. This showed that exercise has a similar effect to counseling on the telomeres of thestressed.If Dr Nelson's work is successfully replicated, it will shine more light on the illunderstood relationship between the health of the mind and the health of the body.
For, as hepoints out, nothing actually changed in the lives of the women in question. They still hadcancer, albeit under treatment, and they were still under stress. Nothing, that is, except theirattitude. (From The Economist, April 9, 2011)Script 43. Exercise and Longevity.Worth all the sweatJust why exercise is so good for people is, at last, being understoodOne sure giveaway of quack medicine is the claim that a product can treat any ailment.There are, sadly, no panaceas.
But some things come close, and exercise is one of them. Asdoctors never tire of reminding people, exercise protects against a host of illnesses, from76heart attacks and dementia to diabetes and infection. How it does so, however, remainssurprisingly mysterious. But a paper just published in Nature by Beth Levine of the Universityof Texas Southwestern Medical Centre and her colleagues sheds some light on the matter.Dr Levine and her team were testing a theory that exercise works its magic, at least inpart, by promoting autophagy.
This process, whose name is derived from the Greek for "selfeating", is a mechanism by which surplus, worn-out or malformed proteins and other cellularcomponents are broken up for scrap and recycled.To carry out the test, Dr Levine turned to those stalwarts of medical research,genetically modified mice. Her first batch of rodents were tweaked so that theirautophagosomes - structures that form around components which have been marked forrecycling-glowed green. After these mice had spent half an hour on a treadmill, she foundthat the number of autophagosomes in their muscles had increased, and it went onincreasing until they had been running for 80 minutes.To find out what, if anything, this exercise-boosted autophagy was doing for mice, theteam engineered a second strain that was unable to respond this way.
Exercise, in otherwords, failed to stimulate their recycling mechanism. When this second group of modifiedmice were tested alongside ordinary ones, they showed less endurance and had less abilityto take up sugar from their bloodstreams.There were longer-term effects, too. In mice, as in people, regular exercise helpsprevent diabetes. But when the team fed their second group of modified mice a diet designedto induce diabetes, they found that exercise gave no protection at all.
Dr Levine and her teamreckon their results suggest that manipulating autophagy may offer a new approach totreating diabetes.And their research is also suggestive in other ways. Autophagy is a hot topic inmedicine, as biologists have come to realize that it helps protect the body from all kinds ofailments.
Autophagy is an ancient mechanism, shared by all eukaryotic organisms (thosewhich, unlike bacteria, keep their DNA in a membrane-bound nucleus within their cells). ltprobably arose as an adaptation to scarcity of nutrients. Critters that can recycle parts ofthemselves for fuel are better able to cope with lean times than those that cannot. But overthe past couple of decades, autophagy has also been shown to be involved in things asdiverse as fighting bacterial infections and slowing the onset of neurological conditions likeAlzheimer's and Huntington's diseases.
Most intriguingly of all, it seems that it can slow theprocess of ageing.Biologists have known for decades that feeding animals near-starvation diets can boosttheir lifespans dramatically. Dr Levine was a member of the team which showed that anincreased level of autophagy, brought on by the stress of living in a constant state of nearstarvation, was the mechanism responsible for this life extension.
The theory is that what arebeing disposed of in particular are worn-out mitochondria. These structures are a cell'spower-packs. They are where glucose and oxygen react together to release energy. Suchreactions, though, often create damaging oxygen-rich molecules called free radicals, whichare thought to be one of the driving forces of ageing. Getting rid of wonky mitochondria wouldreduce free radical production and might thus slow down ageing.A few anti-ageing zealots already subsist on near-starvation diets, but Dr Levine'sresults suggest a similar effect might be gained in a much more agreeable way, via vigorousexercise.
The team's next step is to test whether boosted autophagy can indeed explain thelife-extending effects of exercise. That will take a while. Even in animals as short-lived asmice, she points out, studying ageing is a long-winded process. But she is sufficientlyconfident about the outcome that she has, in the meantime, bought herself a treadmill. (FromThe Economist, January 21, 2012)Script 44. Rejuvenating bodily organsEngaging reverse gearFor the first time, a worn-out organ has been persuaded to renew itself.77Regenerative medicine—the idea that it is possible to revitalise old, dilapidated tissueand keep a body going when its organs start to fail—is attractive. Much effort has thus beenput into creating and nurturing so-called pluripotent stem cells.
These, when appropriatelynudged, can be induced to turn into cells of any other type. They might therefore be used forall sorts of repairs. Pluripotent cells, which once had to be extracted from embryos, can nowbe made routinely from body cells (skin cells, for example). Experiments are going on to seeif, when made from the cells of a particular individual, they might be used to repair damage tothat person’s organs without (as a transplant from someone else would) attracting theattention of his immune system.This approach is promising.
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